Folliculitis is defined histologically as the presence of inflammatory cells within the wall and ostia of the

hair follicle, creating a follicular-based pustule. The type of inflammatory cells varies depending on the
etiology of the folliculitis and/or the stage at which the biopsy specimen was obtained. [1]

In superficial folliculitis, the inflammation is restricted to the infundibular aspect of the follicle, whereas
in deep folliculitis the inflammation not only involves the deeper aspect of the follicle, it also extends
into the surrounding dermis. Deep folliculitis can eventuate from chronic lesions of superficial folliculitis
or from lesions that are manipulated, and may ultimately result in scarring.

Perifolliculitis, on the other hand, is defined as the presence of inflammatory cells, usually lymphocytes,
within the perifollicular tissues with focal extension into the adjacent reticular dermis. Folliculitis and
perifolliculitis can occur independently or together as a result of follicular disruption and irritation.

Acne represents a noninfectious form of folliculitis. Recently there has been a paradigm shift, and the
pathogenesis of acne is now thought to be a primary inflammatory disorder since histology findings have
indicated the presence of perifollicular inflammatory cells even in early stages of acne, preceding the
development of the microcomedone. Hyperkeratinization then results in follicular obstruction, which
allows for sebum accumulation resulting in further distension of the follicle. The normally commensal
bacteria (Propionibacterium acnes) forms a biofilm and its lipases break down sebum triglycerides into
proinflammatory fatty acids and activate the innate immune response through toll-like receptor-2. [2]

Acne-related Medscape articles include Acne Conglobata, Acne Fulminans, Acne Keloidalis Nuchae, Acne
Vulgaris, and Acneiform Eruptions.

Pathophysiology

Folliculitis refers to inflammation of the hair follicle. It can be caused by an infection (bacterial, viral,
fungal, or parasitic) or have a noninfectious etiology, most commonly as the result of follicular trauma,
inflammation, or occlusion.

Eosinophilic folliculitis has a different etiology and is thought to occur as a result of an autoimmune
process directed against the sebocytes or some component of the sebum.
Although the pathophysiology of the acneiform eruption secondary to epidermal growth factor receptor
inhibitors is poorly understood, it is hypothesized that the papulopustular eruption occurs secondary to
inhibition of follicular epidermal differentiation, which eventuates in follicular obstruction and
subsequent inflammation. [3, 4, 5, 6]

Epidemiology

Frequency

Superficial folliculitis is common, but because it is often self-limited and patients rarely present to the
doctor; therefore, the exact incidence is unknown. Those who are seen, more often have either
recurrent or persistent superficial folliculitis or deep folliculitis. Although the incidence is unknown,
conditions that make patients more susceptible include frequent shaving, immunosuppression,
preexisting dermatoses, long-term antibiotic use, occlusive clothing and/or occlusive dressings, exposure
to hot humid temperatures, diabetes mellitus, obesity, and use of EGF-R inhibitor medications.

Folliculitis has also been reported following smallpox or anthrax vaccine. These cases are more common
in military troops who are vaccinated prior to being deployed. [7]

The acneiform eruption attributed to epidermal growth factor receptor inhibitors occurs in 50-100% of
patients and is a dose-dependent drug reaction. [6]

Race

Folliculitis occurs in persons of any race, but pseudofolliculitis and traction folliculitis occurs more
commonly in African Americans, whereas classic eosinophilic folliculitis is more common in Japanese
persons. [8, 9]

Sex

Although most cases of folliculitis show no sex predilection, eosinophilic folliculitis occurs more
frequently in males and Pityrosporum folliculitis is seen slightly more often in females.